ライフサイエンスコーパス: hyperreflexia

1 ite matter dysfunction (i.e., spasticity and hyperreflexia).

2 ndent depression of the H-reflex, suggesting hyperreflexia.

3 tion pressure and fewer episodes of detrusor hyperreflexia.

4 optic atrophy, seizures, and hypertonia with hyperreflexia.

5 a proximal to distal gradient of symptoms of hyperreflexia.

6 s displayed a loss of H-reflex RDD, that is, hyperreflexia.

7 idural stimulation (ES) reduces BDNF-induced hyperreflexia.

8 ng intensities more profoundly (1) decreased hyperreflexia, (2) increased the frequency-dependent mod

9 nce rate in neurological exam was 76 for leg hyperreflexia, 53 for leg weakness, and 37 for Babinski

10 f the monosynaptic H-reflex is indicative of hyperreflexia, a physiological sign of spasticity.

11 creases spinal inhibition and contributes to hyperreflexia after SCI, we investigated the effect of b

12 promising strategy to reduce spasticity and hyperreflexia after SCI.

13 cytic Rac1 contributes to the development of hyperreflexia after SCI.

14 gns of spasticity with the emergence of both hyperreflexia and abnormal involuntary muscle contractio

15 beta neurons as a target population to limit hyperreflexia and enhance locomotor function after SCI.

16 We report two patients with delayed-onset, hyperreflexia and gradually progressive disease.

17 tion of RORbeta neurons reduced BDNF-induced hyperreflexia and improved stepping, similar to ES.

18 's variables, we illustrate the emergence of hyperreflexia and pendular reflexes, reminiscent of neur

19 might have a significant role in post-injury hyperreflexia and plasticity of neighboring neuronal syn

20 ing consequences of post-traumatic autonomic hyperreflexia and post-injury immune suppression.

21 enerative disease characterized primarily by hyperreflexia and progressive spasticity of the lower li

22 rate-dependent depression - an indication of hyperreflexia and spasticity - 1 month following SCI as

23 decreases electrophysiological correlates of hyperreflexia and spasticity in deeply anaesthetized ani

24 ograms because they result in a reduction of hyperreflexia and spasticity.

25 % gestation) are born with muscle stiffness, hyperreflexia and, as recently discovered, increased 5-H

26 er had progressive weakness, fasciculations, hyperreflexia, and active denervation on electromyograph

27 tuations, benefit from sleep, foot dystonia, hyperreflexia, and early susceptibility to levodopa-indu

28 We show that CLP290 decreases hyperreflexia, and reduces muscle co-contraction without

29 ensive care unit with coma, hypersalivation, hyperreflexia, and stimulus-induced clonus.

30 the swing-phase of locomotion in people with hyperreflexia as a result of chronic incomplete SCI.

31 the swing-phase of locomotion in people with hyperreflexia as a result of chronic incomplete SCI.

32 s of neuronal hyperexcitability, and reverse hyperreflexia associated with spasticity after SCI.

33 Hyperreflexia associated with spasticity is a prevalent

34 the sTNFalpha inhibitor prevents sympathetic hyperreflexia-associated splenic atrophy and loss of leu

35 2 receptors, offers a partial explanation of hyperreflexia below a chronic SCI.

36 Hyperreflexia can be caused by several diseases includin

37 Moreover, such sympathetic hyperreflexia detrimentally impacts other effector organ

38 tion parameters for targeting spasticity and hyperreflexia following SCI.

39 ysreflexia, a real-time gauge of sympathetic hyperreflexia, for months postinjury.

40 A non-pharmacological procedure for reducing hyperreflexia has emerged based on operant conditioning

41 Reduced hyperreflexia in astrocytic Rac1KO animals was accompani

42 earance from the synaptic cleft and reducing hyperreflexia in astrocytic Rac1KO animals.

43 Romidepsin treatment reduced signs of hyperreflexia in comparison with control cohorts and in

44 athetic activity and normalizes carotid body hyperreflexia in conscious rats with hypertension; no ef

45 These neurons generate both tonic drive and hyperreflexia in hypertensive (but not normotensive) rat

46 animals, using a battery of tests assessing hyperreflexia in multiple reflex pathways required for n

47 n modulating spastic hypertonia dominated by hyperreflexia in people with chronic stroke and facilita

48 sensation (allodynia) and/or urinary bladder hyperreflexia in the clinical syndrome, interstitial cys

49 t, is used to reduce symptoms of spasticity (hyperreflexia, increases in muscle tone, involuntary mus

50 Hyperreflexia is common after neurological injury such a

51 Thus, reduction of RF hyperreflexia may improve walking function in those with

52 a critical role in the chronic allodynia and hyperreflexia observed after SCI or peripheral nerve dam

53 eborrheic dermatitis, eczema, and persistent hyperreflexia of the lower limbs and with nonsignificant

54 Our previous research has shown that hyperreflexia of the rectus femoris (RF) during pre-swin

55 ings from mice with a range of locomotor and hyperreflexia scores revealed that the excitability of R

56 hreshold intensities preferentially improves hyperreflexia, the frequency-dependent modulation of the

57 ents that prophylactically limit sympathetic hyperreflexia to prevent subsequent effector organ dysfu

58 ysreflexia, a real time gauge of sympathetic hyperreflexia, to prevent associated splenic atrophy.

59 ac1 activity in astrocytes can contribute to hyperreflexia underlying spasticity following SCI.

60 tions ranging from long-term pain to bladder hyperreflexia, we and other groups have sought to develo

61 suggest that toe walking can be generated by hyperreflexia, whereas muscle and neural weaknesses part

62 BDNF) activates hindlimb stepping and causes hyperreflexia, whereas submotor threshold epidural stimu

63 We hypothesized that the reduction in hyperreflexia with exercise after SCI relies on a return

64 n of the RAC1-PAK1 pathway underlying spinal hyperreflexia with SCI-induced spasticity, a feasible dr

65 r and lower limbs, lower limb spasticity and hyperreflexia, with onset in the first decade of life.